Researchers Successfully Reprogram Cancer Cells Back to Benign Cells by Debugging Microprocessor

저자：   업로드：2015-08-26  조회수：

    Cancer is the fiercest disease to human.  Scientists always look for the way to fight cancer.  We have a good news after a lot of research and testing as Mayo Clinic researchers have discovered an unexpected connection between microRNA processing and cell-to-cell adhesion. This connection, the researchers maintain, not only explains the seemingly incongruous presence of adhesion proteins in cancer cells, it also suggests a way to reprogram rogue cancer cells, restoring normal behavior.

    The connection was identified by the researchers when they decided to resolve conflicting reports about the adhesion proteins E-cadherin and p120 catenin. These proteins can help prevent cancer, as part of a growth-inhibiting signal cascade that is activated when cells come into contact with each other. Because of their role in epithelial homeostasis, E-cadherin and p120 catenin have long been considered to be tumor suppressors.

    "However, we and other researchers had found that this hypothesis didn’t seem to be true, since both E-cadherin and p120 are still present in tumor cells and required for their progression," said the Mayo Clinic’s Panos Z. Anastasiadis. Ph.D. "That led us to believe that these molecules have two faces—a good one, maintaining the normal behavior of the cells, and a bad one that drives tumorigenesis."

    Following up on this hunch, a research team led by Dr. Anastasiadis found a crucial link between the adhesion proteins and microRNA-processing machinery that regulates cell growth. The link is a protein called PLEKHA7. The microRNA-processing machinery is the “microprocessor,” a multiprotein complex that can generate microRNAs, which in turn orchestrate whole cellular programs by simultaneously regulating expression of groups of genes.

    The investigators described the link between cell-to-cell adhesion and the microprocessor August 24 in the journal Nature Cell Biology, in an article entitled, “Distinct E-cadherin-based complexes regulate cell behaviour through miRNA processing or Src and p120 catenin activity.” This article holds that when normal cells come in contact with each other, a specific subset of miRNAs suppresses genes that promote cell growth. However, when adhesion is disrupted in cancer cells, these miRNAs are misregulated, and cells grow out of control.

    The article also indicates that restoration of normal miRNA levels in cancer cells might reverse aberrant cell growth.

    “[We identify] two spatially and functionally distinct junctional complexes in non-transformed polarized epithelial cells,” wrote the authors. One complex is growth suppressing. It is at the apical part of normal polarized epithelial cells, the zonula adherens (ZA), and it is defined by the p120 partner PLEKHA7 and a non-nuclear subset of the core microprocessor components DROSHA and DGCR8. The other complex is growth promoting. It is, the autho

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